Colice G L
Clin Chest Med. 1985 Sep;6(3):473-89.
Neurogenic pulmonary edema is an anomaly because it cannot be categorized into either of the two major types of pulmonary edema. Both high-pressure and increased-permeability abnormalities may be involved in the pathogenesis of neurogenic pulmonary edema. Furthermore, the mechanisms responsible for these abnormalities appear quite complex. The high-pressure insult appears to be a function of systemic hypertension, pulmonary venoconstriction, negative and positive inotropic factors, and intrinsic myocardial function. Mediators of the pulmonary endothelial permeability defect have not been defined. Although the high-pressure and increased-permeability abnormalities seem to develop through separate mechanisms, their combined effect is probably synergistic on the accumulation of extravascular lung water. The neurologic pathways responsible for initiating neurogenic pulmonary edema remains a mystery. Despite the questions and uncertainties still surrounding neurogenic pulmonary edema, the substantial progress made in understanding the clinical expression, incidence, and pathogenesis of this syndrome does provide a framework for a reasonable approach to its clinical management.
神经源性肺水肿是一种异常情况,因为它无法被归类为两种主要类型的肺水肿中的任何一种。高压和通透性增加异常都可能参与神经源性肺水肿的发病机制。此外,导致这些异常的机制似乎相当复杂。高压损伤似乎是系统性高血压、肺静脉收缩、正负性肌力因子以及心肌固有功能的作用。肺内皮通透性缺陷的介质尚未明确。尽管高压和通透性增加异常似乎通过不同机制发展,但其联合作用可能对血管外肺水的积聚具有协同作用。引发神经源性肺水肿的神经通路仍是一个谜。尽管围绕神经源性肺水肿仍存在诸多问题和不确定性,但在理解该综合征的临床表现、发病率和发病机制方面取得的实质性进展确实为其临床管理的合理方法提供了一个框架。